Hypoglycaemic, antioxidative and nephroprotective effects of taurine in alloxan diabetic rabbits

Winiarska, Katarzyna; Szymański, Konrad M.; Górniak, Patryk; Dudziak, Marta; Bryła, Jadwiga

doi:10.1016/j.biochi.2008.09.006

Cited by 102 publications

(62 citation statements)

References 67 publications

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“…Previous studies of Winiarska et al (2009) reported Tau-mediated, diminished NOX activity in the kidney cortex of alloxan diabetic rabbits. Tau-mediated NOX activation in other cell types might be underlying the widely recognized antioxidant action of this amino acid as cited in numerous reports (Huxtable 1992;Schuller-Levis and Park 2003;Oprescu et al 2007).…”

Section: Discussionmentioning

confidence: 84%

Taurine in adipocytes prevents insulin-mediated H2o2 generation and activates Pka and lipolysis

et al. 2011

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Among many actions assigned to taurine (Tau), the most abundant amino acid in numerous mammalian tissues, it prevents high-fat diet-induced obesity with increasing resting energy expenditure. To sustain this Tau action, the goal of the present study was to explore the acute effects of Tau on baseline and on adrenaline, insulin and their second messengers to modulate lipolysis in white adipose tissue (WAT) cells from rat epididymis. The Tau effects in this topic were compared with those recorded with Gly, Cys and Met. Tau on its own did not modify baseline lipolysis. Tau raised isoproterenol- and dibutyryl-cAMP (Bt2cAMP)-activated glycerol release. Gly diminished Bt2cAMP-activated glycerol release, and Cys and Met had no effect. Cyclic AMP-dependent activation of protein kinase A (PKA) in cell-free extracts decreased slightly by Gly and was unaltered by Cys, Met, and Tau. PKA catalytic activity in cell-free extracts was stimulated by Tau and unchanged by Cys, Gly and Met. Gly and Tau effects on PKA disappeared when these amino acids were withdrawn by gel filtration. Insulin-mediated NADPH-oxidase (NOX) raises H2O2 pool, which promotes PKA subunit oxidation, and precludes its cAMP activation; thus, lipolysis is diminished. Tau, but not Cys, Gly and Met, inhibited, by as much as 70%, insulin-mediated H2O2 pool increase. These data suggested that Tau raised lipolysis in adipocytes by two mechanisms: stimulating cAMP-dependent PKA catalytic activity and favoring PKA activation by cAMP as a consequence of lowering the H2O2 pool.

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Section: Discussionmentioning

confidence: 84%

Taurine in adipocytes prevents insulin-mediated H2o2 generation and activates Pka and lipolysis

et al. 2011

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“…-ATPase activity and reduced TNF-a as well as NO production in kidney during various toxin and drug-induced pathophysiological conditions (Das et al 2010c;Roy et al 2009;Manna et al 2009b). The anti-hyperglycemic and nephroprotective roles of taurine in diabetes have already been reported (Winiarska et al 2009;Das et al 2011a;Franconi et al 2006;Gavrovskaya et al 2008). Besides, very limited in vivo and in vitro studies have demonstrated that the protective effect of taurine on diabetic kidney is mediated via suppression of AGEs, TGFb and ROS (Winiarska et al 2009;Nandhini and Anuradha 2003;Higo et al 2008).…”

Section: Introductionmentioning

confidence: 97%

“…Kidney does not depend on insulin for glucose uptake; thus the increased plasma glucose levels in diabetes will also result in high intracellular levels of glucose and face severe and sustained hyperglycemia (Chandra et al 2002). Evidence suggests that hyperglycemia is associated with increased production of reactive oxygen species (ROS) and the resulting oxidative stress is thought to play a key role in the pathogenesis of this disorder (Winiarska et al 2009). The possible enzymatic and non-enzymatic sources of ROS in the diabetic kidney are autoxidation of glucose, transition metal-catalyzed Fenton reactions, advanced glycation end products (AGEs), polyol pathway flux, mitochondrial respiratory chain deficiencies, xanthine oxidase activity, peroxidases, nitric oxide synthase (NOS) and NAD(P)H oxidase (Forbes et al 2008).…”

Section: Introductionmentioning

confidence: 99%

Taurine ameliorates alloxan-induced diabetic renal injury, oxidative stress-related signaling pathways and apoptosis in rats

2012

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Hyperglycemia-induced oxidative stress plays a vital role in the progression of diabetic nephropathy. The renoprotective nature of taurine has also been reported earlier; but little is known about the mechanism of this beneficial action. The present study has, therefore, been carried out to explore in detail the mechanism of the renoprotective effect of taurine under diabetic conditions. Diabetes was induced in rats by alloxan (single i.p. dose of 120 mg/kg body weight) administration. Taurine was administered orally for 3 weeks (1% w/v in drinking water) either from the day on which alloxan was injected or after the onset of diabetes. Alloxan-induced diabetic rats showed a significant increase in plasma glucose, enhanced the levels of renal damage markers, plasma creatinine, urea nitrogen and urinary albumin. Diabetic renal injury was associated with increased kidney weight to body weight ratio and glomerular hypertrophy. Moreover, it increased the productions of reactive oxygen species, enhanced lipid peroxidation and protein carbonylation in association with decreased intracellular antioxidant defense in the kidney tissue. In addition, hyperglycemia enhanced the levels of proinflammatory cytokins (TNF-α, IL-6, IL-1β) and Na(+)--K(+)-ATPase activity with a concomitant reduction in NO content and eNOS expression in diabetic kidney. Investigation of the oxidative stress-responsive signaling cascades showed the upregulation of PKCα, PKCβ, PKCε and MAPkinases in the renal tissue of the diabetic animals. However, taurine administration decreased the elevated blood glucose and proinflammatory cytokine levels, reduced renal oxidative stress (via decrease in xanthine oxidase activity, AGEs formation and inhibition of p47phox/CYP2E1 pathways), improved renal function and protected renal tissue from alloxan-induced apoptosis via the regulation of Bcl-2 family and caspase-9/3 proteins. Taurine supplementation in regular diet could, therefore, be beneficial to regulate diabetes-associated renal complications.

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“…21,22 Furthermore, administration of certain amino acids shown to attenuates DN in experimental animals. [23][24][25] Literature lucid with evidence showed that L-glutamine (LG) possesses potent antiulcer, antioxidant, anti-bacterial, cardioprotective, anticancer, hepatoprotective, and anti-apoptotic potential. [26][27][28][29] It has been reported that LG significantly attenuated cisplatin-induced genotoxicity.…”

Section: Introductionmentioning

confidence: 99%

Protective effect ofL-glutamine against diabetes-induced nephropathy in experimental animal: Role of KIM-1, NGAL, TGF-β1, and collagen-1

Sadar¹,

Kaspate

Vyawahare³

2016

Renal Failure

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Diabetic nephropathy is a serious microvascular complication and one of the main causes of endstage renal disease. L-Glutamine (LG) is naturally occurring amino acids with antidiabetic and antioxidant potential. The aim of present investigation was to evaluate the potential of LG against streptozotocin (STZ)-induced diabetic nephropathy (DN) in laboratory rats. DN was induced in male Wistar rats (200-220 g) by intraperitoneal administration of STZ (55 mg/kg). Animals were treated orally with either distilled water (10 mg/kg) or LG (250, 500, and 1000 mg/kg) or Sitagliptin (5 mg/kg). Various biochemical, molecular, and histological (hematoxylin-eosin and Masson's trichrome stain) parameters were assessed. Administration of LG (500 and 1000 mg/kg) significantly inhibited (p < .05) STZ-induced alterations in serum and urine biochemistry (urine creatinine, uric acid, albumin, and BUN). It also significantly increased creatinine clearance rate. STZ induced increase in renal oxidonitrosative stress was significantly decreased (p < .05) by LG (500 and 1000 mg/kg) treatment. Upregulated renal KIM-1, NGAL, TGF-b1, and collagen-1 mRNA expression after STZ administration was significantly inhibited (p < .05) by LG (500 and 1000 mg/ kg) treatment. Correlation analysis also revealed that antidiabetic potential of LG attenuates STZinduced elevated renal KIM-1, NGAL, TGF-b1, and collagen-1 mRNA expression. Histopathological alteration induced by STZ in renal tissue was ameliorated by LG treatment. In conclusion, results of present investigation suggest that treatment with LG ameliorated STZ-induced DN via the inhibition of oxidonitrosative stress as well as downregulation of KIM-1, NGAL, TGF-b1, and collagen-1 mRNA expressions. ARTICLE HISTORY

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Hypoglycaemic, antioxidative and nephroprotective effects of taurine in alloxan diabetic rabbits

Cited by 102 publications

References 67 publications

Taurine in adipocytes prevents insulin-mediated H2o2 generation and activates Pka and lipolysis

Taurine in adipocytes prevents insulin-mediated H2o2 generation and activates Pka and lipolysis

Taurine ameliorates alloxan-induced diabetic renal injury, oxidative stress-related signaling pathways and apoptosis in rats

Protective effect ofL-glutamine against diabetes-induced nephropathy in experimental animal: Role of KIM-1, NGAL, TGF-β1, and collagen-1

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